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Introduction: advances in antiviral therapy for chronic hepatitis C infection—the influence of genotype and HIV co-infection

Nature Clinical Practice Gastroenterology & Hepatology volume 4, pages S1–S2 (2007)Cite this article

It is estimated that 180 million people worldwide and 5 million people in the US are infected with hepatitis C virus (HCV).1 In the US, most individuals infected with HCV have not been diagnosed. The majority of HCV-infected individuals will develop chronic HCV infection, with up to 30% developing cirrhosis over a 30-year period. Of those with cirrhosis, between 1.5% and 4% annually will develop hepatocellular carcinoma. Factors promoting the progression or severity of HCV infection include a high level of alcohol intake, age above 40 years at time of infection, coinfection with human immunodeficiency virus (HIV), chronic hepatitis B virus coinfection, and male sex.1

At present, no safe and effective vaccines exist for preventing HCV infection. A sustained viral response (SVR) is attainable in approximately 50% of subjects with chronic HCV infection taking a combination of pegylated interferon and ribavirin.2 Unfortunately, combination therapy is expensive and associated with significant side effects, so only about 10% of individuals diagnosed with chronic HCV infection have received treatment. HCV genotype is a major determinant of response to combination therapy.3 Approximately 70% of individuals in the US known to be chronically infected with HCV have genotype 1, approximately 15% have genotype 2, and 6–7% genotype 3; the genotype of the remaining 8–9% is unknown. In previously untreated chronic HCV infection, combination therapy produces a SVR in about 45% of individuals with genotype 1 and in 70–80% of individuals with genotypes 2 or 3.

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References

  1. Viral Hepatitis Resource Center. [http://www.cdc.gov/ncidod/diseases/hepatitis/resource/index.htm] (Accessed 2 October 2006)

  2. Manns MP et al. (2006) Treating viral hepatitis C: efficacy, side effects and complications. Gut 55: 1350–1359

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  1. University of Miami School of Medicine, 1500 NW 12 Avenue, Jackson Medical Tower E-1101, Miami, FL 33136, USA eschiff@med.miami.edu

Authors and Affiliations

  1. Division of Hepatology; and Director, ER Schiff is Leonard Miller Professor of Medicine; Chief, Center for Liver Disease, University of Miami School of Medicine, Miami, FL, USA.,

    Eugene R Schiff

  2. Division of Hepatology, Chief, Division of Hepatology,

    Eugene R Schiff

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  1. Eugene R Schiff
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Competing interests

Eugene R Schiff acts as a consultant to Abbott, Achillion Pharmaceutical, Bayer, Bristol Myers Squibb, Cadence Pharmaceuticals, Gilead, GlobeImmune Inc., Idenix, Maxim, National Genetics Institute, Novartis, Ortho-Biotech, Pfizer, PowerMed Ltd., Prometheus, Roche Molecular, Sankyo Pharma Inc., Schering-Plough, and SciClone Pharmaceuticals. He has received grant support from Abbott, Bayer, Bristol Myers Squibb, Coley, Gilead, GlaxoSmithKline, Idenix, Ortho-Biotech, Prometheus, Roche Diagnostics, Roche Molecular, Roche Pharmaceutical, Schering-Plough, SciClone Pharmaceuticals, and Vertex Pharamceuticals. He also receives honoraria for speaking from Abbott, Bristol Myers Squibb, Giliead, GlaxoSmithKline, Idenix, Ortho-Biotech, and Schering-Plough.

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Schiff, E. Introduction: advances in antiviral therapy for chronic hepatitis C infection—the influence of genotype and HIV co-infection. Nat Rev Gastroenterol Hepatol 4 (Suppl 1), S1–S2 (2007). https://doi.org/10.1038/ncpgasthep0690

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